ABSTRACT
RESUMEN Introducción: La inflamación es una respuesta homeostática del organismo. Es uno de los principales motivos de consulta en Cuba y el mundo. Existe una percepción errónea de que es una entidad aislada y siempre patológica. Es un proceso dinámico, complejo, sistémico y multifactorial. Por eso constituye un reto el dilucidar los elementos, cambios tisulares que causa y cómo proceder en la clínica ante un cuadro inflamatorio. Objetivo: Describir la inflamación, su clasificación, elementos involucrados y cambios sistémicos desde una perspectiva inmunológica. Material y Métodos: Se realizó una revisión sobre el tema empleando la bibliografía actualizada y luego se consultaron artículos de libre acceso en las bases de datos Pubmed y Scielo en el período de enero de 2013 a diciembre de 2018. Desarrollo: La inflamación puede clasificarse según el daño, tiempo o los efectores involucrados. Las principales moléculas son las citocinas como TNF-α, IFN-γ, IL-1β, IL-10, IL-6, TGF-β. Participan células como los neutrófilos, mastocitos, macrófagos, linfocitos T y las del endotelio vascular. Durante el proceso inflamatorio se modifican las funciones de casi todos los sistemas de órganos. En ciertos tipos de inflamación, es la respuesta adaptativa quien origina y perpetúa el proceso inflamatorio. Conclusiones: En la actualidad se desconocen los acontecimientos que desencadenan inflamación crónica y cómo ocurre el daño tisular. El mayor desafío consiste en dilucidar las causas y mecanismos inmunológicos que conllevan a las manifestaciones inflamatorias sistémicas que se manifiestan como enfermedades neurológicas, cardiovasculares y autoinmunes, entre otras.
ABSTRACT Introduction: Inflammation is a homeostatic response of the body. It is one of the main reasons for consultation in Cuba and throughout world. There is a misperception that it is an isolated and always pathological entity. It is a dynamic, complex, systemic, and multifactorial process. Therefore, it is a challenge to elucidate the elements and the tissue changes that it causes to establish the best way to improve the clinical practice related to an inflammatory process. Objective: To describe inflammation, its classification, elements involved, and systemic changes from an immunological perspective. Material and Methods: A review of the topic was made using the updated bibliography. Free-access articles were consulted in Pubmed and Scielo databases in the period from January 2013 to December 2018. Development: Inflammation can be classified according to the damage, time or effectors involved. The main molecules are the cytokines like TNF-α, IFN-γ, IL-1β, IL-10, IL-6, TGF-β. Some cells participate such as neutrophils, mastocytes, macrophages, T-lymphocyes, and the vascular endothelium. During the inflammatory process, the functions of almost all organ systems are modified. It produces systemic changes that are observed in physiological processes such as pregnancy or aging. Sometimes inflammation triggers diseases such as cardiovascular and neurological ones, and cancer. The pathophysiological mechanisms have not been clarified. Conclusions: Currently, the events that trigger chronic inflammation and how tissue damage occurs are unknown. The biggest challenge is to elucidate the causes and immunological mechanisms that lead to inflammatory manifestations that are expressed as systemic neurological, cardiovascular and autoimmune diseases, among others.
Subject(s)
Humans , History, 21st Century , Inflammation/immunology , BibliographyABSTRACT
According to the expansion of lifespan, neuronal disorder based on inflammation has been social problem. Therefore, we isolated shikonin from Lithospermum erythrorhizon and evaluated anti-inflammatory effects of shikonin in lipopolysaccharide (LSP)-stimulated BV2 microglial cells. Shikonin dose-dependently inhibits the expression of the proinflammatory mediators, nitric oxide (NO), prostaglandin E2 (PGE2), and tumor necrosis factor-alpha (TNF-alpha) as well as their main regulatory genes and products such as inducible NO synthase (iNOS), cyclooxygenase-2 (COX-2), and TNF-alpha in LPS-stimulated BV2 microglial cells. Additionally, shikonin suppressed the LPS-induced DNA-binding activity of nuclear factor-kappaB (NF-kappaB) to regulate the key regulatory genes of the proinflammatory mediators, such as iNOS, COX-2, and TNF-alpha, accompanied with downregulation of reactive oxygen species (ROS) generation. The results indicate that shikonin may downregulate the expression of proinflammatory genes involved in the synthesis of NO, PGE2, and TNF-alpha in LPS-treated BV2 microglial cells by suppressing ROS and NF-kappaB. Taken together, our results revealed that shikonin exerts downregulation of proinflammatory mediators by interference the ROS and NF-kappaB signaling pathway.
Subject(s)
Cyclooxygenase 2 , Dinoprostone , Down-Regulation , Genes, Regulator , Inflammation , Lithospermum , Neurons , NF-kappa B , Nitric Oxide , Nitric Oxide Synthase , Reactive Oxygen Species , Social Problems , Tumor Necrosis Factor-alphaABSTRACT
Objective: To investigate the anti-inflammatory effects of Jeju seaweeds on macrophage RAW 264.7 cells under lipopolysaccharide (LPS) stimulation.Methods:Ethyl acetate fractions were prepared from five different types of Jeju seaweeds, Dictyopteris divaricata (D. divaricata), Dictyopteris prolifera (D. prolifera), Prionitis cornea (P. cornea), Grateloupia lanceolata (G. lanceolata), and Grateloupia filicina (G. filicina). They were screened for inhibitory effects on proinflammatory mediators and cytokines such as nitric oxide (NO), prostaglandin E2, tumor necrosis factor-α (TNF-α), and interleukin-6 (IL-6).Results:Our results revealed that D. divaricata, D. prolifera, P. cornea, G. lanceolata, and G. filicina potently inhibited LPS-stimulated NO production (IC50 values were 18.0, 38.36, 38.43, 32.81 and 37.14 μg/mL, respectively). Consistent with these findings, D. divaricata, D. prolifera, P. cornea, and G. filicina also reduced the LPS-induced and prostaglandin E2 production in a concentration-dependent manner. Expectedly, they suppressed the expression of inducible NO synthase and cyclooxygenase-2 at the protein level in a dose-dependent manner in the RAW 264.7 cells, as determined by western blotting. In addition, the levels of TNF-α and IL-6, released into the medium, were also reduced by D. divaricata, D. prolifera, P. cornea, G. lanceolata, andG. filicina in a dose-dependent manner (IC 50 values for TNF-α were 16.11, 28.21, 84.27, 45.52 and 74.75 μg/mL, respectively; IC50 values for IL-6 were 37.35, 80.08, 103.28, 62.53 and 84.28 μg/mL, respectively). The total phlorotannin content was measured by the Folin-Ciocalteu method and expressed as phloroglucinol equivalents. The content was 92.0 μg/mg for D. divaricata, 151.8 μg/mg for D. prolifera, 57.2 μg/mg for P. cornea, 53.0 μg/mg for G. lanceolata, and 40.2 μg/mg for G.filicina. Conclusions: Thus, these findings suggest that Jeju seaweed extracts have potential therapeutic applications for inflammatory responses.
ABSTRACT
<p><b>OBJECTIVE</b>To investigate the anti-inflammatory effects of Jeju seaweeds on macrophage RAW 264.7 cells under lipopolysaccharide (LPS) stimulation.</p><p><b>METHODS</b>Ethyl acetate fractions were prepared from five different types of Jeju seaweeds, Dictyopteris divaricata (D. divaricata), Dictyopteris prolifera (D. prolifera), Prionitis cornea (P. cornea), Grateloupia lanceolata (G. lanceolata), and Grateloupia filicina (G. filicina). They were screened for inhibitory effects on proinflammatory mediators and cytokines such as nitric oxide (NO), prostaglandin E2, tumor necrosis factor-α (TNF-α), and interleukin-6 (IL-6).</p><p><b>RESULTS</b>Our results revealed that D. divaricata, D. prolifera, P. cornea, G. lanceolata, and G. filicina potently inhibited LPS-stimulated NO production (IC50 values were 18.0, 38.36, 38.43, 32.81 and 37.14 µg/mL, respectively). Consistent with these findings, D. divaricata, D. prolifera, P. cornea, and G. filicina also reduced the LPS-induced and prostaglandin E2 production in a concentration-dependent manner. Expectedly, they suppressed the expression of inducible NO synthase and cyclooxygenase-2 at the protein level in a dose-dependent manner in the RAW 264.7 cells, as determined by western blotting. In addition, the levels of TNF-α and IL-6, released into the medium, were also reduced by D. divaricata, D. prolifera, P. cornea, G. lanceolata, and G. filicina in a dose-dependent manner (IC50 values for TNF-α were 16.11, 28.21, 84.27, 45.52 and 74.75 µg/mL, respectively; IC50 values for IL-6 were 37.35, 80.08, 103.28, 62.53 and 84.28 µg/mL, respectively). The total phlorotannin content was measured by the Folin-Ciocalteu method and expressed as phloroglucinol equivalents. The content was 92.0 µg/mg for D. divaricata, 151.8 µg/mg for D. prolifera, 57.2 µg/mg for P. cornea, 53.0 µg/mg for G. lanceolata, and 40.2 µg/mg for G. filicina.</p><p><b>CONCLUSIONS</b>Thus, these findings suggest that Jeju seaweed extracts have potential therapeutic applications for inflammatory responses.</p>
ABSTRACT
Objective: To investigate the anti-inflammatory effects of Jeju seaweeds on macrophage RAW 264.7 cells under lipopolysaccharide (LPS) stimulation. Methods: Ethyl acetate fractions were prepared from five different types of Jeju seaweeds, Dictyopteris divaricata (D. divaricata), Dictyopteris prolifera (D. prolifera), Prionitis cornea (P. cornea), Grateloupia lanceolata (G. lanceolata), and Grateloupia filicina (G. filicina). They were screened for inhibitory effects on proinflammatory mediators and cytokines such as nitric oxide (NO), prostaglandin E
ABSTRACT
AIM: To observe the effect of antibiotic treatment on the inflammatory mediator expression in peritoneum and the peritoneal transport function in rats with acute peritonitis, and explore its mechanisms. METHODS: Eighty-six SD rats were randomly divided into three groups. Control group (n=28) were treated with PBS (ip), peritonitis group (n=28) and treatment group (n=28) were challenged with the E.coli (ip), but at 3 h and 9 h gentamicin was given (ip) in treatment group. Seven rats of every group were randomly sacrificed at 24 h, 48 h, 72 h and 7 d. Peritoneal equilibration test (PET) was did before they were killed. Leukocyte count, pathological changes and the expression of CD45, NF-?B, IL-1?, TNF-? in peritoneum were examined. RESULTS: (1)The blood leukocytes in peritonitis group decreased strikingly, but did not change obviously in other two groups. The peritoneal fluid leukocytes in peritonitis group increased significantly from 24 h to 72 h, while in treatment group, it enhanced more strikingly than peritonitis group at 24 h, and recovered earlier. (2) Both in peritonitis group and treatment group, the expression of activated NF-?B, IL-1?, TNF-? and CD45 increased significantly, but the treatment group was lower than model group at 48 h and 72 h. The mRNA level of IL-1? and TNF-? had the same trend as their protein expression. (3) Compared with the control group, UF and D/D_0 Glu decreased significantly in model group and treatment group, and D/PTP increased dramatically. The D/P TP in treatment group lowered obviously compared with peritonitis group, while the net UF and D/D_0 Glu had not significant difference between treatment group and model group. CONCLUSION: Antibiotic treatment can partly decrease the expression of inflammatory mediators in peritoneum of rats with acute peritonitis and also can improve the protein transport ability to some extent, but can not improve the peritoneal ultrafiltration and the glucose transport function.